Evidence map›Paper›PMID 30154415›Full record

ArticleScientific reports2018

Serum from patients with chronic obstructive pulmonary disease induces senescence-related phenotype in bronchial epithelial cells.

Barbara Kuźnar-Kamińska, Justyna Mikuła-Pietrasik, Anna Witucka, Aleksandra Romaniuk, Natalia Konieczna, Błażej Rubiś, Krzysztof Książek, Andrzej Tykarski, Halina Batura-Gabryel

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In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed.

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  16. Cellular Senescence in the Kidney.Journal of the American Society of Nephrology : JASN · 2019
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Barbara Kuźnar-KamińskaDepartment of Pulmonology, Allergology and Respiratory Oncology, Poznań University of Medical Sciences, Szamarzewskiego 84 Str., 60-569, Poznań, Poland. kaminska@ump.edu.pl.
Justyna Mikuła-PietrasikDepartment of Hypertensiology, Angiology and Internal Medicine, Poznań University of Medical Sciences, Długa 1/2 Str., 61-848, Poznań, Poland.
Anna WituckaDepartment of Hypertensiology, Angiology and Internal Medicine, Poznań University of Medical Sciences, Długa 1/2 Str., 61-848, Poznań, Poland.
Aleksandra RomaniukDepartment of Clinical Chemistry and Molecular Diagnostics, Poznan University of Medical Sciences, Przybyszewskiego 49 Str., 60-355, Poznań, Poland.
Natalia KoniecznaDepartment of Clinical Chemistry and Molecular Diagnostics, Poznan University of Medical Sciences, Przybyszewskiego 49 Str., 60-355, Poznań, Poland.
Błażej RubiśDepartment of Clinical Chemistry and Molecular Diagnostics, Poznan University of Medical Sciences, Przybyszewskiego 49 Str., 60-355, Poznań, Poland.ORCID 0000-0003-1730-0176
Krzysztof KsiążekDepartment of Hypertensiology, Angiology and Internal Medicine, Poznań University of Medical Sciences, Długa 1/2 Str., 61-848, Poznań, Poland.
Andrzej TykarskiDepartment of Hypertensiology, Angiology and Internal Medicine, Poznań University of Medical Sciences, Długa 1/2 Str., 61-848, Poznań, Poland.
Halina Batura-GabryelDepartment of Pulmonology, Allergology and Respiratory Oncology, Poznań University of Medical Sciences, Szamarzewskiego 84 Str., 60-569, Poznań, Poland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is a risk factor for the development of lung cancer (LC). The mechanism of interplay between both diseases remains poorly recognized. This report examines whether COPD may cause a senescence response in human bronchial epithelial cells (HBECs), leading to the progression of LC in a senescence-dependent manner. The results show that HBECs exposed to serum from COPD patients manifest increased expression of markers of cellular senescence, including senescence-associated β-galactosidase (SA-β-Gal), histone γ-H2A.X, and p21, as compared to the serum of healthy donors. This effect coincides with an increased generation of reactive oxygen species by these cells. The clinical analysis demonstrated that COPD may cause the senescence, independently on smoking status and disease severity. The concentrations of CXCL5, CXCL8/IL-8 and VEGF were higher in conditioned medium (CM) harvested from HBECs after exposure to COPD serum as compared to controls. In addition, CM treated with serum from COPD patients stimulated adhesion of A549 cancer cells to HBECs, as well as accelerating cancer cell proliferation and migration in vitro. Collectively, these findings indicate that COPD may induce senescence-like changes in HBECs and thus enhance some processes associated with the progression of lung cancer.

Indexed as

Cellular SenescenceSerumAgedAged, 80 and overAntigens, DifferentiationBronchiCells, CulturedCytokinesEpithelial CellsFemaleHumansMaleMiddle AgedPulmonary Disease, Chronic ObstructiveAntigens, DifferentiationCytokines

Identifiers

PMID30154415
PMCPMC6113312

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.